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      Early life household intactness and timing of pubertal onset in girls: a prospective cohort study

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          Abstract

          Background

          Girls who experience early-life familial stress may have heightened risk of early puberty, which has adverse implications for adolescent and adult health. We assessed the association between household intactness and pubertal onset using a racially/ethnically diverse cohort of girls from Northern California.

          Methods

          A prospective cohort study of 26,044 girls born in 2003-10. Girls living with both parents from birth up to 6 years were considered to come from “intact” households while others constituted “non-intact” households. Pubertal development was measured using pediatrician-assessed Tanner staging for breast and pubic hair. Pubertal onset was defined as the transition from Tanner Stage 1 to 2+ for breast (thelarche) and pubic hair (pubarche). Menarche data was collected from routine well-child questionnaires. Weibull regression models accommodating left, right, and interval censoring were used to determine risk of earlier thelarche and pubarche, and logistic regressions were used to assess the risk of early menarche (age < 12).

          Results

          Girls exposed to non-intact households before age 2 years were at increased risk for earlier thelarche and pubarche with significant effect modification by race/ethnicity, compared with girls from intact households. The associations were strongest among Black girls (adjusted hazard ratio [HR]: 1.60, 95% confidence interval [CI]: 1.29,1.98; HR: 1.42, 95%CI: 1.15,1.77 for thelarche and pubarche, respectively). There were no significant associations among Asian/Pacific Islanders. Girls who lived in non-intact households before age 2 years were also at increased risk for earlier menarche, but without race/ethnic interaction. Adjustment for prepubertal obesity did not change these associations. Associations between living in non-intact households after age 2 years and early puberty were weaker but still significant.

          Conclusions

          Exposure to a non-intact household early in life may increase the risk of early puberty in girls. Future psychosocial interventions focused on improving family cohesiveness and efforts to reduce childhood stress among families that are non-intact may mitigate these negative associations, thereby preventing future adverse health effects of early puberty and health disparities.

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          Most cited references 33

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          Timing of pubertal maturation in girls: an integrated life history approach.

           Bruce Ellis (2004)
          Life history theory provides a metatheoretical framework for the study of pubertal timing from an evolutionary-developmental perspective. The current article reviews 5 middle-level theories--energetics theory, stress-suppression theory, psychosocial acceleration theory, paternal investment theory, and child development theory--each of which applies the basic assumptions of life history theory to the question of environmental influences on timing of puberty in girls. These theories converge in their conceptualization of pubertal timing as responsive to ecological conditions but diverge in their conceptualization of (a) the nature, extent, and direction of environmental influences and (b) the effects of pubertal timing on other reproductive variables. Competing hypotheses derived from the 5 perspectives are evaluated. An extension of W. T. Boyce and B. J. Ellis's (in press) theory of stress reactivity is proposed to account for both inhibiting and accelerating effects of psychosocial stress on timing of pubertal development. This review highlights the multiplicity of (often unrecognized) perspectives guiding research, raises challenges to virtually all of these, and presents an alternative framework in an effort to move research forward in this arena of multidisciplinary inquiry.
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            Variations in pattern of pubertal changes in girls.

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              Public health implications of altered puberty timing.

              Changes in puberty timing have implications for the treatment of individual children, for the risk of later adult disease, and for chemical testing and risk assessment for the population. Children with early puberty are at a risk for accelerated skeletal maturation and short adult height, early sexual debut, potential sexual abuse, and psychosocial difficulties. Altered puberty timing is also of concern for the development of reproductive tract cancers later in life. For example, an early age of menarche is a risk factor for breast cancer. A low age at male puberty is associated with an increased risk for testicular cancer according to several, but not all, epidemiologic studies. Girls and, possibly, boys who exhibit premature adrenarche are at a higher risk for developing features of metabolic syndrome, including obesity, type 2 diabetes, and cardiovascular disease later in adulthood. Altered timing of puberty also has implications for behavioral disorders. For example, an early maturation is associated with a greater incidence of conduct and behavior disorders during adolescence. Finally, altered puberty timing is considered an adverse effect in reproductive toxicity risk assessment for chemicals. Recent US legislation has mandated improved chemical testing approaches for protecting children's health and screening for endocrine-disrupting agents, which has led to changes in the US Environmental Protection Agency's risk assessment and toxicity testing guidelines to include puberty-related assessments and to the validation of pubertal male and female rat assays for endocrine screening.
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                Author and article information

                Contributors
                sara.aghaee@kp.org
                jdeardorff@berkeley.edu
                Louise.C.Greenspan@kp.org
                Charles.Quesenberry@kp.org
                Larry.Kushi@kp.org
                Ai.Kubo@kp.org
                Journal
                BMC Pediatr
                BMC Pediatr
                BMC Pediatrics
                BioMed Central (London )
                1471-2431
                28 October 2020
                28 October 2020
                2020
                : 20
                Affiliations
                [1 ]GRID grid.280062.e, ISNI 0000 0000 9957 7758, Kaiser Permanente Division of Research, ; 2000 Broadway, CA 94612 Oakland, USA
                [2 ]GRID grid.47840.3f, ISNI 0000 0001 2181 7878, Division of Maternal and Child Health, School of Public Health, , University of California, ; 2121 Berkeley Way #5302, CA 94720 Berkeley, USA
                [3 ]GRID grid.414890.0, ISNI 0000 0004 0461 9476, Kaiser Permanente San Francisco Medical Center, ; 2425 Geary Boulevard, CA 94115 San Francisco, USA
                Article
                2345
                10.1186/s12887-020-02345-w
                7592583
                33109126
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000009, Foundation for the National Institutes of Health;
                Award ID: K07CA166143
                Funded by: FundRef http://dx.doi.org/10.13039/100000009, Foundation for the National Institutes of Health;
                Award ID: R01HD098220
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2020

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